Mitochondria are required for pro-ageing features of the senescent phenotype. - Test2 - elhamkhani - TriplyDB

Mitochondria are required for pro-ageing features of the senescent phenotype.

Mitochondria are required for pro-ageing features of the senescent phenotype.

http://www.wikidata.org/entity/Q34046100

about

MicroRNA-Regulated Proinflammatory Cytokines in Sarcopenia Connecting the Dots: From DNA Damage and Repair to Aging Mitochondria Initiate and Regulate Sarcopenia Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism Cellular senescence drives age-dependent hepatic steatosis.Persistent mTORC1 signaling in cell senescence results from defects in amino acid and growth factor sensing.Induction of autophagy by ARHI (DIRAS3) alters fundamental metabolic pathways in ovarian cancer models Mitochondrial Aging: Is There a Mitochondrial Clock?From Ancient Pathways to Aging Cells-Connecting Metabolism and Cellular Senescence.Old age and the associated impairment of bones' adaptation to loading are associated with transcriptomic changes in cellular metabolism, cell-matrix interactions and the cell cycle.53BP1 contributes to regulation of autophagic clearance of mitochondria.Mitochondrial fusion, fission, and mitochondrial toxicity.Quantifying intracellular rates of glycolytic and oxidative ATP production and consumption using extracellular flux measurements.Targeting the SASP to combat ageing: Mitochondria as possible intracellular allies?Oxidative stress and ageing.Telomeres and Cell Senescence - Size Matters Not.Mitochondria in Cell Senescence: Is Mitophagy the Weakest Link?A disease with a sweet tooth: exploring the Warburg effect in Alzheimer's disease.Decreased mTOR signalling reduces mitochondrial ROS in brain via accumulation of the telomerase protein TERT within mitochondria.Lipid (per) oxidation in mitochondria: an emerging target in the ageing process?Demystifying the role of mitochondria in senescence.PGC-1 Coactivators: Shepherding the Mitochondrial Biogenesis of Tumors.Mitophagy Transcriptome: Mechanistic Insights into Polyphenol-Mediated Mitophagy.Aging and Caloric Restriction Research: A Biological Perspective With Translational Potential.Systems modelling ageing: from single senescent cells to simple multi-cellular models.Mitochondria and senescence: new actors for an old play.Senescence in the aging process.Powering senescence: The ugly side of mitochondria.Dysregulation of mTORC1/autophagy axis in senescence.Detecting senescence: a new method for an old pigment.Mitochondrial Functional Changes Characterization in Young and Senescent Human Adipose Derived MSCs.Replicatively senescent human fibroblasts reveal a distinct intracellular metabolic profile with alterations in NAD+ and nicotinamide metabolism.Autophagy impairment with lysosomal and mitochondrial dysfunction is an important characteristic of oxidative stress-induced senescence.Pink1 and Parkin regulate Drosophila intestinal stem cell proliferation during stress and aging.The role of mitochondrial ROS in the aging brain.SIRT4 interacts with OPA1 and regulates mitochondrial quality control and mitophagy.The senescent bystander effect is caused by ROS-activated NF-κB signalling.Age-dependent changes in inflammation and extracellular matrix in bovine oviduct epithelial cells during the post-ovulatory phase.Targeted elimination of senescent Ras-transformed cells by suppression of MEK/ERK pathway.Cellular Senescence in Age-Related Macular Degeneration: Can Autophagy and DNA Damage Response Play a Role?

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Mitochondria are required for pro-ageing features of the senescent phenotype.

http://www.wikidata.org/entity/Q34046100

description

2016 nî lūn-bûn

@nan

2016 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2016 թվականի փետրվարին հրատարակված գիտական հոդված

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2016年の論文

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2016年論文

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2016年論文

@zh-hant

2016年論文

@zh-hk

2016年論文

@zh-mo

2016年論文

@zh-tw

2016年论文

@wuu

name

Mitochondria are required for pro-ageing features of the senescent phenotype.

@ast

Mitochondria are required for pro-ageing features of the senescent phenotype.

@en

Mitochondria are required for pro-ageing features of the senescent phenotype.

@nl

type

label

Mitochondria are required for pro-ageing features of the senescent phenotype.

@ast

Mitochondria are required for pro-ageing features of the senescent phenotype.

@en

Mitochondria are required for pro-ageing features of the senescent phenotype.

@nl

prefLabel

Mitochondria are required for pro-ageing features of the senescent phenotype.

@ast

Mitochondria are required for pro-ageing features of the senescent phenotype.

@en

Mitochondria are required for pro-ageing features of the senescent phenotype.

@nl

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The EMBO Journal

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Mitochondria are required for pro-ageing features of the senescent phenotype

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Alina Merz

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Clara Correia-Melo

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Derek Mann

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Francisco D M Marques

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Graeme Hewitt

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Jodie Birch

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John Cole

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Michael D Rushton

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Michelle Charles

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Mohammad Bohlooly-Y

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P2860

TopHat2: accurate alignment of transcriptomes in the presence of insertions, deletions and gene fusions

PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1

Feedback between p21 and reactive oxygen production is necessary for cell senescence

Superoxide dismutase 1 knock-down induces senescence in human fibroblasts

Parkin is recruited selectively to impaired mitochondria and promotes their autophagy

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

Myopathy caused by mammalian target of rapamycin complex 1 (mTORC1) inactivation is not reversed by restoring mitochondrial function

mTOR signaling in growth control and disease

Rapamycin fed late in life extends lifespan in genetically heterogeneous mice

A mitochondrial protein compendium elucidates complex I disease biology

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724-742

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10.15252/EMBJ.201592862

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7

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35

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Douglas R. Green

Gabriele Saretzki

Viktor Korolchuk

Thomas von Zglinicki

Giovanni Quarato

Rafal Czapiewski

Bernadette Carroll

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2016-02-04T00:00:00Z

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26848154

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